Watanabe M, Suzuki J, Suzuki H
Department of Pediatrics, Fukushima Medical College, Japan.
Nihon Jinzo Gakkai Shi. 1996 Aug;38(8):356-63.
For the purpose of clarifying the changes occurring in thromboxane (TX)A2 metabolism in the platelet of nephrosis patients, we investigated the changes in platelet sensitivity to TXA2 and the changes in TXA2 production in pediatric patients with nephrotic syndrome (N.S.) using STA2 which is an analogue of TXA2 and ONO 3708 which is a TXA2 receptor antagonist. The subjects investigated in the present study consisted of 11 cases with initial onset of N.S. (onset group), 15 relapse patients (relapse group) and 15 children with N.S. without any recurrence in the past 6 months (remission group) as well as 25 normal children (control group). The results were as follows: (1) Platelet aggregation attributable to STA2 stimulation was enhanced at the onset and relapse of N.S. (2) Sensitivity to TXA2 was enhanced in the platelets of patients in the relapse group. (3) Though some demonstrated enhanced platelet sensitivity to TXA2, while others in the onset group did not, enhanced sensitivity was observed in all the patients along with an improvement in hypoalbuminemia. (4) The amount of daily urinary excretion of TXB2 and 11-dehydro-TXB2 in the onset group and relapse group was increased in comparison with the status in the remission group and control group. The above results demonstrated enhanced platelet sensitivity to TXA2 and increased biological production of TXA2 in patients with N.S., suggesting that TXA2 metabolism in the platelet is deeply involved in the pathophysiology of N.S.
为阐明肾病患者血小板中血栓素(TX)A2代谢的变化,我们使用TX A2类似物STA2和TX A2受体拮抗剂ONO 3708,研究了肾病综合征(N.S.)患儿血小板对TX A2的敏感性变化以及TX A2生成的变化。本研究调查的对象包括11例初发N.S.患者(发病组)、15例复发患者(复发组)、15例过去6个月无任何复发的N.S.患儿(缓解组)以及25名正常儿童(对照组)。结果如下:(1)在N.S.发病和复发时,STA2刺激引起的血小板聚集增强。(2)复发组患者血小板对TX A2的敏感性增强。(3)虽然发病组中一些患者表现出血小板对TX A2的敏感性增强,而另一些患者则没有,但随着低白蛋白血症的改善,所有患者均观察到敏感性增强。(4)发病组和复发组TXB2和11 -脱氢 - TXB2的每日尿排泄量与缓解组和对照组相比增加。上述结果表明,N.S.患者血小板对TX A2的敏感性增强且TX A2的生物生成增加,提示血小板中的TX A2代谢与N.S.的病理生理学密切相关。